Cardiac support device with anti-fibrosis coating

ABSTRACT

A jacket of biological compatible material has an internal volume dimensioned for an apex of the heart to be inserted into the volume and for the jacket to be slipped over the heart. The jacket has a longitudinal dimension between upper and lower ends sufficient for the jacket to surround a lower portion of the heart with the jacket surrounding a valvular annulus of the heart and further surrounding the lower portion to cover at least the ventricular lower extremities of the heart. The jacket is adapted to be secured to the heart with the jacket surrounding at least the valvular annulus and the ventricular lower extremities. The jacket is adjustable on the heart to snugly conform to an external geometry of the heart and assume a maximum adjusted volume for the jacket to constrain circumferential expansion of the heart beyond the maximum adjusted volume during diastole and to permit unimpeded contraction of the heart during systole.

REFERENCE TO RELATED APPLICATION

This application is a division of application Ser. No. 10/810,096, filedMar. 26, 2004, which is a continuation of application Ser. No.09/880,576, filed Jun. 13, 2001, which is a continuation of applicationSer. No. 09/565,621, filed May 4, 2000 (now U.S. Pat. No. 6,537,203,issued Mar. 25, 2003), which is a continuation of application Ser. No.09/114,510, filed Jul. 13, 1998 (now U.S. Pat. No. 6,123,662, issuedSep. 26, 2000), which are hereby incorporated by reference in theirentirety.

TECHNICAL FIELD

The present invention pertains to a device and method for treating heartdisease. More particularly, the present invention is directed to amethod and device for treating congestive heart disease and relatedvalvular dysfunction.

BACKGROUND OF THE INVENTION

Congestive heart disease is a progressive and debilitating illness. Thedisease is characterized by a progressive enlargement of the heart.

As the heart enlarges, the heart is performing an increasing amount ofwork in order to pump blood each heart beat. In time, the heart becomesso enlarged the heart cannot adequately supply blood. An afflictedpatient is fatigued, unable to perform even simple exerting tasks andexperiences pain and discomfort. Further, as the heart enlarges, theinternal heart valves cannot adequately close. This impairs the functionof the valves and further reduces the heart's ability to supply blood.

Causes of congestive heart disease are not fully known. In certaininstances, congestive heart disease may result from viral infections. Insuch cases, the heart may enlarge to such an extent that the adverseconsequences of heart enlargement continue after the viral infection haspassed and the disease continues its progressively debilitating course.

Patients suffering from congestive heart disease are commonly groupedinto four classes (i.e., Classes I, II, III and IV). In the early stages(e.g., Classes I and II), drug therapy is the commonly proscribedtreatment. Drug therapy treats the symptoms of the disease and may slowthe progression of the disease. Importantly, there is no cure forcongestive heart disease. Even with drug therapy, the disease willprogress. Further, the drugs may have adverse side effects.

Presently, the only permanent treatment for congestive heart disease isheart transplant. To qualify, a patient must be in the later stage ofthe disease (e.g., Classes III and IV with Class IV patients givenpriority for transplant). Such patients are extremely sick individuals.Class III patients have marked physical activity limitations and ClassIV patients are symptomatic even at rest.

Due to the absence of effective intermediate treatment between drugtherapy and heart transplant, Class III and IV patients will havesuffered terribly before qualifying for heart transplant. Further, aftersuch suffering, the available treatment is unsatisfactory. Hearttransplant procedures are very risky, extremely invasive and expensiveand only shortly extend a patient's life. For example, prior totransplant, a Class IV patient may have a life expectancy of 6 months toone-year. Heart transplant may improve the expectancy to about fiveyears.

Unfortunately, not enough hearts are available for transplant to meetthe needs of congestive heart disease patients. In the United States, inexcess of 35,000 transplant candidates compete for only about 2,000transplants per year. A transplant waiting list is about 8-12 monthslong on average and frequently a patient may have to wait about 1-2years for a donor heart. While the availability of donor hearts hashistorically increased, the rate of increase is slowing dramatically.Even if the risks and expense of heart transplant could be tolerated,this treatment option is becoming increasingly unavailable. Further,many patient's do not qualify for heart transplant for failure to meetany one of a number of qualifying criteria.

Congestive heart failure has an enormous societal impact. In the UnitedStates alone, about five million people suffer from the disease (ClassesI through IV combined). Alarmingly, congestive heart failure is one ofthe most rapidly accelerating diseases (about 400,000 new patients inthe United States each year). Economic costs of the disease have beenestimated at $38 billion annually.

Not surprising, substantial effort has been made to find alternativetreatments for congestive heart disease. Recently, a new surgicalprocedure has been developed. Referred to as the Batista procedure, thesurgical technique includes dissecting and removing portions of theheart in order to reduce heart volume. This is a radical new andexperimental procedure subject to substantial controversy. Furthermore,the procedure is highly invasive, risky and expensive and commonlyincludes other expensive procedures (such as a concurrent heart valvereplacement). Also, the treatment is limited to Class IV patients and,accordingly, provides no hope to patients facing ineffective drugtreatment prior to Class IV. Finally, if the procedure fails, emergencyheart transplant is the only available option.

Clearly, there is a need for alternative treatments applicable to bothearly and later stages of the disease to either stop the progressivenature of the disease or more drastically slow the progressive nature ofcongestive heart disease. Unfortunately, currently developed options areexperimental, costly and problematic.

Cardiomyoplasty is a recently developed treatment for earlier stagecongestive heart disease (e.g., as early as Class III dilatedcardiomyopathy). In this procedure, the latissimus dorsi muscle (takenfrom the patient's shoulder) is wrapped around the heart and chronicallypaced synchronously with ventricular systole. Pacing of the muscleresults in muscle contraction to assist the contraction of the heartduring systole.

While cardiomyoplasty has resulted in symptomatic improvement, thenature of the improvement is not understood. For example, one study hassuggested the benefits of cardiomyoplasty are derived less from activesystolic assist than from remodeling, perhaps because of an externalelastic constraint. The study suggests an elastic constraint (i.e., anon-stimulated muscle wrap or an artificial elastic sock placed aroundthe heart) could provide similar benefits. Kass et al., ReverseRemodeling From Cardiomyoplasty In Human Heart Failure: ExternalConstraint Versus Active Assist, 91 Circulation 2314-2318 (1995).

Even though cardiomyoplasty has demonstrated symptomatic improvement,studies suggest the procedure only minimally improves cardiacperformance. The procedure is highly invasive requiring harvesting apatient's muscle and an open chest approach (i.e., sternotomy) to accessthe heart. Furthermore, the procedure is expensive—especially thoseusing a paced muscle. Such procedures require costly pacemakers. Thecardiomyoplasty procedure is complicated. For example, it is difficultto adequately wrap the muscle around the heart with a satisfactory fit.Also, if adequate blood flow is not maintained to the wrapped muscle,the muscle may necrose. The muscle may stretch after wrapping reducingits constraining benefits and is generally not susceptible topost-operative adjustment. Finally, the muscle may fibrose and adhere tothe heart causing undesirable constraint on the contraction of the heartduring systole.

In addition to cardiomyoplasty, mechanical assist devices have beendeveloped as intermediate procedures for treating congestive heartdisease. Such devices include left ventricular assist devices (“LVAD”)and total artificial hearts (“TAH”). An LVAD includes a mechanical pumpfor urging blood flow from the left ventricle and into the aorta. Anexample of such is shown in U.S. Pat. No. 4,995,857 to Arnold dated Feb.26, 1991. LVAD surgeries are still in U.S. clinical trials and notgenerally available. Such surgeries are expensive. The devices are atrisk of mechanical failure and frequently require external powersupplies. TAH devices, such as the celebrated Jarvik heart, are used astemporary measures while a patient awaits a donor heart for transplant.

Other attempts at cardiac assist devices are found in U.S. Pat. No.4,957,477 to Lundbäck dated Sep. 18, 1990, U.S. Pat. No. 5,131,905 toGrooters dated Jul. 21, 1992 and U.S. Pat. No. 5,256,132 to Snydersdated Oct. 26, 1993. Both of the Grooters and Snyders patents teachcardiac assist devices which pump fluid into chambers opposing the heartto assist systolic contractions of the heart. The Lundbäck patentteaches a double-walled jacket surrounding the heart. A fluid fills achamber between the walls of the jacket. The inner wall is positionedagainst the heart and is pliable to move with the heart. Movement of theheart during beating displaces fluid within the jacket chamber.

Commonly assigned U.S. Pat. No. 5,702,343 to Alferness dated Dec. 30,1997 teaches a jacket to constrain cardiac expansion during diastole.The present invention pertains to improvements to the inventiondisclosed in the '343 patent.

SUMMARY OF THE INVENTION

According to a preferred embodiment of the present invention, a methodand device are disclosed for treating congestive heart disease andrelated cardiac complications such as valvular disorders. The inventionincludes a jacket of biologically compatible material. The jacket has aninternal volume dimensioned for an apex of the heart to be inserted intothe volume and for the jacket to be slipped over the heart. The jackethas a longitudinal dimension between upper and lower ends sufficient forthe jacket to surround a lower portion of the heart with the jacketsurrounding a valvular annulus of the heart and further surrounding thelower portion to cover at least the ventricular lower extremities of theheart. The jacket is adapted to be secured to the heart with the jacketsurrounding at least the valvular annulus and the ventricular lowerextremities. The jacket is adjustable on the heart to snugly conform toan external geometry of the heart and assume a maximum adjusted volumefor the jacket to constrain circumferential expansion of the heartbeyond the maximum adjusted volume during diastole and to permitunimpeded contraction of the heart during systole. In one embodiment, alower end of the jacket can be secured to the patient's diaphragm afterplacement around the heart.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a schematic cross-sectional view of a normal, healthy humanheart shown during systole;

FIG. 1A is the view of FIG. 1 showing the heart during diastole;

FIG. 1B is a view of a left ventricle of a healthy heart as viewed froma septum and showing a mitral valve;

FIG. 2 is a schematic cross-sectional view of a diseased human heartshown during systole;

FIG. 2A is the view of FIG. 2 showing the heart during diastole;

FIG. 2B is the view of FIG. 1B showing a diseased heart;

FIG. 3 is a perspective view of a first embodiment of a cardiacconstraint device according to the present invention;

FIG. 3A is a side elevation view of a diseased heart in diastole withthe device of FIG. 3 in place;

FIG. 4 is a perspective view of a second embodiment of a cardiacconstraint device according to the present invention;

FIG. 4A is a side elevation view of a diseased heart in diastole withthe device of FIG. 4 in place;

FIG. 5 is a cross-sectional view of a device of the present inventionoverlying a myocardium and with the material of the device gathered fora snug fit;

FIG. 6 is an enlarged view of a knit construction of the device of thepresent invention in a rest state; and

FIG. 7 is a schematic view of the material of FIG. 6.

DETAILED DESCRIPTION OF THE INVENTION

With initial reference to FIGS. 1 and 1A, a normal, healthy human heartH′ is schematically shown in cross-section and will now be described inorder to facilitate an understanding of the present invention. In FIG.1, the heart H′ is shown during systole (i.e., high left ventricularpressure). In FIG. 1A, the heart H′ is shown during diastole (i.e., lowleft ventricular pressure).

The heart H′ is a muscle having an outer wall or myocardium MYO′ and aninternal wall or septum S′. The myocardium MYO′ and septum S′ definefour internal heart chambers including a right atrium RA′, a left atriumLA′, a right ventricle RV′ and a left ventricle LV′. The heart H′ has alength measured along a longitudinal axis AA′-BB′ from an upper end orbase B′ to a lower end or apex A′.

The right and left atria RA′, LA′ reside in an upper portion UP′ of theheart H′ adjacent the base B′. The right and left ventricles RV′, LV′reside in a lower portion LP′ of the heart H′ adjacent the apex A′. Theventricles RV′, LV′ terminate at ventricular lower extremities LE′adjacent the apex A′ and spaced therefrom by the thickness of themyocardium MYO′.

Due to the compound curves of the upper and lower portions UP′, LP′, theupper and lower portions UP′, LP′ meet at a circumferential groovecommonly referred to as the A-V groove AVG′. Extending away from theupper portion UP′ are a plurality of major blood vessels communicatingwith the chambers RA′, RV′, LA′, LV′. For ease of illustration, only thesuperior vena cava SVC′ and a left pulmonary vein LPV′ are shown asbeing representative.

The heart H′ contains valves to regulate blood flow between the chambersRA′, RV′, LA′, LV′ and between the chambers and the major vessels (e.g.,the superior vena cava SVC′ and a left pulmonary vein LPV′). For ease ofillustration, not all of such valves are shown. Instead, only thetricuspid valve TV′ between the right atrium RA′ and right ventricle RV′and the mitral valve MV′ between the left atrium LA′ and left ventricleLV′ are shown as being representative.

The valves are secured, in part, to the myocardium MYO′ in a region ofthe lower portion LP′ adjacent the A-V groove AVG′ and referred to asthe valvular annulus VA′. The valves TV′ and MV′ open and close throughthe beating cycle of the heart H.

FIGS. 1 and 1A show a normal, healthy heart H′ during systole anddiastole, respectively. During systole (FIG. 1), the myocardium MYO′ iscontracting and the heart assumes a shape including a generally conicallower portion LP′. During diastole (FIG. 1A), the heart H′ is expandingand the conical shape of the lower portion LP′ bulges radially outwardly(relative to axis AA′-BB′).

The motion of the heart H′ and the variation in the shape of the heartH′ during contraction and expansion is complex. The amount of motionvaries considerably throughout the heart H′. The motion includes acomponent which is parallel to the axis AA′-BB′ (conveniently referredto as longitudinal expansion or contraction). The motion also includes acomponent perpendicular to the axis AA′-BB′ (conveniently referred to ascircumferential expansion or contraction).

Having described a healthy heart H′ during systole (FIG. 1) and diastole(FIG. 1A), comparison can now be made with a heart deformed bycongestive heart disease. Such a heart H is shown in systole in FIG. 2and in diastole in FIG. 2A. All elements of diseased heart H are labeledidentically with similar elements of healthy heart H′ except only forthe omission of the apostrophe in order to distinguish diseased heart Hfrom healthy heart H′.

Comparing FIGS. 1 and 2 (showing hearts H′ and H during systole), thelower portion LP of the diseased heart H has lost the tapered conicalshape of the lower portion LP′ of the healthy heart H′. Instead, thelower portion LP of the diseased heart H bulges outwardly between theapex A and the A-V groove AVG. So deformed, the diseased heart H duringsystole (FIG. 2) resembles the healthy heart H′ during diastole (FIG.1A). During diastole (FIG. 2A), the deformation is even more extreme.

As a diseased heart H enlarges from the representation of FIGS. 1 and 1Ato that of FIGS. 2 and 2A, the heart H becomes a progressivelyinefficient pump. Therefore, the heart H requires more energy to pumpthe same amount of blood. Continued progression of the disease resultsin the heart H being unable to supply adequate blood to the patient'sbody and the patient becomes symptomatic insufficiency.

For ease of illustration, the progression of congestive heart diseasehas been illustrated and described with reference to a progressiveenlargement of the lower portion LP of the heart H. While suchenlargement of the lower portion LP is most common and troublesome,enlargement of the upper portion UP may also occur.

In addition to cardiac insufficiency, the enlargement of the heart H canlead to valvular disorders. As the circumference of the valvular annulusVA increases, the leaflets of the valves TV and MV may spread apart.After a certain amount of enlargement, the spreading may be so severethe leaflets cannot completely close (as illustrated by the mitral valveMV in FIG. 2A). Incomplete closure results in valvular regurgitationcontributing to an additional degradation in cardiac performance. Whilecircumferential enlargement of the valvular annulus VA may contribute tovalvular dysfunction as described, the separation of the valve leafletsis most commonly attributed to deformation of the geometry of the heartH. This is best described with reference to FIGS. 1B and 2B.

FIGS. 1B and 2B show a healthy and diseased heart, respectively, leftventricle LV′, LV during systole as viewed from the septum (not shown inFIGS. 1B and 2B). In a healthy heart H′, the leaflets MVL′ of the mitralvalve MV′ are urged closed by left ventricular pressure. The papillarymuscles PM′, PM are connected to the heart wall MYO′, MYO, near thelower ventricular extremities LE′, LE. The papillary muscles PM′, PMpull on the leaflets MVL′, MVL via connecting chordae tendineae CT′, CT.Pull of the leaflets by the papillary muscles functions to prevent valveleakage in the normal heart by holding the valve leaflets in a closedposition during systole. In the significantly diseased heart H, theleaflets of the mitral valve may not close sufficiently to preventregurgitation of blood from the ventricle LV to the atrium duringsystole.

As shown in FIG. 1B, the geometry of the healthy heart H′ is such thatthe myocardium MYO′, papillary muscles PM′ and chordae tendineae CT′cooperate to permit the mitral valve MV′ to fully close. However, whenthe myocardium MYO bulges outwardly in the diseased heart H (FIG. 2B),the bulging results in displacement of the papillary muscles PM. Thisdisplacement acts to pull the leaflets MVL to a displaced position suchthat the mitral valve cannot fully close.

Having described the characteristics and problems of congestive heartdisease, the treatment method and apparatus of the present inventionwill now be described.

In general, a jacket of the invention is configured to surround themyocardium MYO. As used herein, “surround” means that jacket providesreduced expansion of the heart wall during diastole by applyingconstraining surfaces at least at diametrically opposing aspects of theheart. In some preferred embodiments disclosed herein, the diametricallyopposed surfaces are interconnected, for example, by a continuousmaterial that can substantially encircle the external surface of theheart.

With reference-now to FIGS. 3, 3A, 4 and 4A, the device of the presentinvention is shown as a jacket 10 of flexible, biologically compatiblematerial. The jacket 10 is an enclosed knit material having upper andlower ends 12, 14. The jacket 10, 10′ defines an internal volume 16, 16′which is completely enclosed but for the open ends 12, 12′ and 14′. Inthe embodiment of FIG. 3, lower end 14 is closed. In the embodiment ofFIG. 4, lower end 14′ is open. In both embodiments, upper ends 12, 12′are open. Throughout this description, the embodiment of FIG. 3 will bediscussed. Elements in common between the embodiments of FIGS. 3 and 4are numbered identically with the addition of an apostrophe todistinguish the second embodiment and such elements need not beseparately discussed.

The jacket 10 is dimensioned with respect to a heart H to be treated.Specifically, the jacket 10 is sized for the heart H to be constrainedwithin the volume 16. The jacket 10 can be slipped around the heart H.The jacket 10 has a length L between the upper and lower ends 12, 14sufficient for the jacket 10 to constrain the lower portion LP. Theupper end 12 of the jacket 10 extends at least to the valvular annulusVA and further extends to the lower portion LP to constrain at least thelower ventricular extremities LE.

Since enlargement of the lower portion LP is most troublesome, in apreferred embodiment, the jacket 10 is sized so that the upper end 12can reside in the A-V groove AVG. Where it is desired to constrainenlargement of the upper portion UP, the jacket 10 may be extended tocover the upper portion UP.

Sizing the jacket 10 for the upper end 12 to terminate at the A-V grooveAVG is desirable for a number of reasons. First, the groove AVG is areadily identifiable anatomical feature to assist a surgeon in placingthe jacket 10. By placing the upper end 12 in the A-V groove AVG, thesurgeon is assured the jacket 10 will provide sufficient constraint atthe valvular annulus VA. The A-V groove AVG and the major vessels act asnatural stops for placement of the jacket 10 while assuring coverage ofthe valvular annulus VA. Using such features as natural stops isparticularly beneficial in minimally invasive surgeries where asurgeon's vision may be obscured or limited.

When the parietal pericardium is opened, the lower portion LP is free ofobstructions for applying the jacket 10 over the apex A. If, however,the parietal pericardium is intact, the diaphragmatic attachment to theparietal pericardium inhibits application of the jacket over the apex Aof the heart. In this situation, the jacket can be opened along a lineextending from the upper end 12′ to the lower end 14′ of jacket 10′. Thejacket can then be applied around the pericardial surface of the heartand the opposing edges of the opened line secured together after placedon the heart. Systems for securing the opposing edges are disclosed in,for example, U.S. Pat. No. 5,702,343, the entire disclosure of which isincorporated herein by reference. The lower end 14′ can then be securedto the diaphragm or associated tissues using, for example, sutures,staples, etc.

In the embodiment of FIGS. 3 and 3A, the lower end 14 is closed and thelength L is sized for the apex A of the heart H to be received withinthe lower end 14 when the upper end 12 is placed at the A-V groove AVG.In the embodiment of FIGS. 4 and 4A, the lower end 14′ is open and thelength L′ is sized for the apex A of the heart H to protrude beyond thelower end 14′ when the upper end 12′ is placed at the A-V groove AVG.The length L′ is sized so that the lower end 14′ extends beyond thelower ventricular extremities LE such that in both of jackets 10, 10′,the myocardium MYO surrounding the ventricles RV, LV is in directopposition to material of the jacket 10, 10′. Such placement isdesirable for the jacket 10, 10′ to present a constraint againstenlargement of the ventricular walls of the heart H.

After the jacket 10 is positioned on the heart H as described above, thejacket 10 is secured to the heart. Preferably, the jacket 10 is securedto the heart H through sutures. The jacket 10 is sutured to the heart Hat suture locations S circumferentially spaced along the upper end 12.While a surgeon may elect to add additional suture locations to preventshifting of the jacket 10 after placement, the number of such locationsS is preferably limited so that the jacket 10 does not restrictcontraction of the heart H during systole.

To permit the jacket 10 to be easily placed on the heart H, the volumeand shape of the jacket 10 are larger than the lower portion LP duringdiastole. So sized, the jacket 10 may be easily slipped around the heartH. Once placed, the jacket's volume and shape are adjusted for thejacket 10 to snugly conform to the external geometry of the heart Hduring diastole. Such sizing is easily accomplished due to the knitconstruction of the jacket 10. For example, excess material of thejacket 10 can be gathered and sutured S″ (FIG. 5) to reduce the volumeof the jacket 10 and conform the jacket 10 to the shape of the heart Hduring diastole. Such shape represents a maximum adjusted volume. Thejacket 10 constrains enlargement of the heart H beyond the maximumadjusted volume while preventing restricted contraction of the heart Hduring systole. As an alternative to gathering of FIG. 5, the jacket 10can be provided with other ways of adjusting volume. For example, asdisclosed in U.S. Pat. No. 5,702,343, the jacket can be provided with aslot. The edges of the slot can be drawn together to reduce the volumeof the jacket.

The jacket 10 is adjusted to a snug fit on the heart H during diastole.Care is taken to avoid tightening the jacket 10 too much such thatcardiac function is impaired. During diastole, the left ventricle LVfills with blood. If the jacket 10 is too tight, the left ventricle LVcannot adequately expand and left ventricular pressure will rise. Duringthe fitting of the jacket 10, the surgeon can monitor left ventricularpressure. For example, a well-known technique for monitoring so-calledpulmonary wedge pressure uses a catheter placed in the pulmonary artery.The wedge pressure provides an indication of filling pressure in theleft atrium LA and left ventricle LV. While minor increases in pressure(e.g., 2-3 mm Hg) can be tolerated, the jacket 10 is snugly fit on theheart H but not so tight as to cause a significant increase in leftventricular pressure during diastole.

As mentioned, the jacket 10 is constructed from a knit, biocompatiblematerial. The knit 18 is illustrated in FIG. 6. Preferably, the knit isa so-called “Atlas knit” well known in the fabric industry. The Atlasknit is described in Paling, Warp Knitting Technology, p. 111, ColumbinePress (Publishers) Ltd., Buxton, Great Britain (1970).

The Atlas knit is a knit of fibers 20 having directional expansionproperties. More specifically, the knit 18, although formed of generallyinelastic fibers 20, permits a construction of a flexible fabric atleast slightly expandable beyond a rest state. FIG. 6 illustrates theknit 18 in a rest state. The fibers 20 of the fabric 18 are woven intotwo sets of fiber strands 21 a, 21 b having longitudinal axes X_(a) andX_(b). The strands 21 a, 21 b are interwoven to form the fabric 18 withstrands 21 a generally parallel and spaced-apart and with strands 21 bgenerally parallel and spaced-apart.

For ease of illustration, fabric 18 is schematically shown in FIG. 7with the axis of the strands 21 a, 21 b only being shown. The strands 21a, 21 b are interwoven with the axes X_(a) and X_(b) defining adiamond-shaped open cell 23 having diagonal axes A_(m). In a preferredembodiment, the axes A_(m) are 5 mm in length when the fabric 18 is atrest and not stretched. The fabric 18 can stretch in response to aforce. For any given force, the fabric 18 stretches most when the forceis applied parallel to the diagonal axes A_(m). The fabric 18 stretchesleast when the force is applied parallel to the strand axes X_(a) andX_(b). The jacket 10 is constructed for the material of the knit to bedirectionally aligned for a diagonal axis A_(m) to be parallel to theheart's longitudinal axis AA-BB

While the jacket 10 is expandable due to the above described knitpattern, the fibers 20 of the knit 18 are preferably non-expandable.While all materials expand to at least a small amount, the fibers 20 arepreferably formed of a material with a low modulus of elasticity. Inresponse to the low pressures in the heart H during diastole, the fibers20 are non-elastic. In a preferred embodiment, the fibers are 70 Denierpolyester. While polyester is presently preferred, other suitablematerials include polytetrafluoroethylene (PTFE), expanded PTFE (ePTFE),polypropylene and stainless steel.

The knit material has numerous advantages. Such a material is flexibleto permit unrestricted-movement of the heart H other than the desiredconstraint on circumferential expansion). The material is open defininga plurality of interstitial spaces for fluid permeability as well asminimizing the amount of surface area of direct contact between theheart H and the material of the jacket 10 (thereby minimizing areas ofirritation or abrasion) to minimize fibrosis and scar tissue.

The open areas of the knit construction also allows for electricalconnection between the heart and surrounding tissue for passage ofelectrical current to and from the heart. For example, although the knitmaterial is an electrical insulator, the open knit construction issufficiently electrically permeable to permit the use of trans-chestdefibrillation of the heart. Also, the open, flexible constructionpermits passage of electrical elements (e.g., pacer leads) through thejacket. Additionally, the open construction permits other procedures,e.g., coronary bypass, to be performed without removal of the jacket.

A large open area for cells 23 is desirable to minimize the amount ofsurface area of the heart H in contact with the material of the jacket10 (thereby reducing fibrosis). However, if the cell area 23 is toolarge, localized aneurysm can form. Also, a strand 21 a, 21 b can overlya coronary vessel with sufficient force to partially block the vessel. Asmaller cell size increases the number of strands thereby decreasing therestricting force per strand. Preferably, a maximum cell area is nogreater than about 6.45 cm² (about 2.54 cm by 2.54 cm) and, morepreferably, is about 0.25 cm² (about 0.5 cm by 0.5 cm). The maximum cellarea is the area of a cell 23 after the material of the jacket 10 isfully stretched and adjusted to the maximum adjusted volume on the heartH as previously described.

The fabric 18 is preferably tear and run resistant. In the event of amaterial defect or inadvertent tear, such a defect or tear is restrictedfrom propagation by reason of the knit construction.

With the foregoing, a device and method have been taught to treatcardiac disease. The jacket 10 constrains further undesirablecircumferential enlargement of the heart while not impeding other motionof the heart H. With the benefits of the present teachings, numerousmodifications are possible. For example, the jacket 10 need not bedirectly applied to the epicardium (i.e., outer surface of themyocardium) but could be placed over the parietal pericardium. Further,an anti-fibrosis lining (such as a PTFE coating on the fibers of theknit) could be placed between the heart H and the jacket 10.Alternatively, the fibers 20 can be coated with PTFE coating 20′.

The jacket 10 is low-cost, easy to place and secure, and is susceptibleto use in minimally invasive procedures. The thin, flexible fabric 18permits the jacket 10 to be collapsed and passed through a smalldiameter tube in a minimally invasive procedure.

The jacket 10 can be used in early stages of congestive heart disease.For patients facing heart enlargement due to viral infection, the jacket10 permits constraint of the heart H for a sufficient time to permit theviral infection to pass. In addition to preventing further heartenlargement, the jacket 10 treats valvular disorders by constrainingcircumferential enlargement of the valvular annulus and deformation ofthe ventricular walls.

The jacket 10, including the knit construction, freely permitslongitudinal and circumferential contraction of the heart H (necessaryfor heart function). Unlike a solid wrap (such as a muscle wrap in acardiomyoplasty procedure), the fabric 18 does not impede cardiaccontraction. After fitting, the jacket 10 is inelastic to preventfurther heart enlargement while permitting unrestricted inward movementof the ventricular walls. The open cell structure permits access tocoronary vessels for bypass procedures subsequent to placement of thejacket 10. Also, in cardiomyoplasty, the latissimus dorsi muscle has avariable and large thickness (ranging from about 1 mm to 1 cm). Thematerial of the jacket 10 is uniformly thin (less than 1 mm thick). Thethin wall construction is less susceptible to fibrosis and minimizesinterference with cardiac contractile function.

Animal test studies on the device show the efficacy of the invention.Test animals were provided with the device 10 of FIG. 3. The animals'hearts were rapidly paced to induce enlargement. After six weeks,animals without the device experienced significant heart enlargementwhile those with the device experienced no significant enlargement.Further, animals with the device had significantly reduced mitral valveregurgitation.

In addition to the foregoing, the present invention can be used toreduce heart size at the time of placement in addition to preventingfurther enlargement. For example, the device can be placed on the heartand sized snugly to urge the heart to a reduced size. More preferably,the heart size can be reduced at the time of jacket placement throughdrugs (e.g., dobutamine, dopamine or epinephrine or any other positiveinotropic agents) to reduce the heart size. The jacket of the presentinvention is then snugly placed on the reduced sized heart and preventsenlargement beyond the reduced size.

From the foregoing, a low cost, reduced risk method and device aretaught to treat cardiac disease. The invention is adapted for use withboth early and later stage congestive heart disease patients. Theinvention reduces the enlargement rate of the heart as well as reducingcardiac valve regurgitation.

1. A method for treating a disease of a heart, the method comprising:(a) selecting a device including: a jacket constructed of a plurality offlexible elongated members interconnected to form a jacket material,wherein at least a portion of the individual elongated members arecoated with an anti-fibrosis coating, and wherein said jacket is adaptedto be placed on said heart, said material is dimensioned so as toconform to an external geometry of said heart surrounding at least theventricles to constrain circumferential expansion of said heart duringdiastole and permit substantially unimpeded contraction of said heartduring systole; (b) placing said jacket on said heart with said materialsurrounding at least the ventricles of said heart to constraincircumferential expansion of said heart during diastole and permitsubstantially unimpeded contraction of said heart during systole.
 2. Amethod according to claim 1 wherein said elongated members are formed ofmetal.
 3. A method according to claim 2, wherein said metal is stainlesssteel.
 4. A method according to claim 1, wherein said jacket is placedover an epicardial surface of said heart.
 5. A method according to claim1, wherein said jacket is placed over a pericardium.
 6. A methodaccording to claim 1, wherein said jacket is adapted to constrain saidheart from expanding beyond a maximum volume.